Vasopressin V1a Receptor Signaling in a Rat Choroid Plexus Cell Line

Battle, Thierry; Preisser, Laurence; Marteau, V.; Meduri, Géri; Lambert, Mary P.; Nitschke, Roland; Brown, Petra; Corman, B.

doi:10.1006/bbrc.2000.3301

Cited by 8 publications

(4 citation statements)

References 32 publications

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“…However, Johanson and coworkers showed a dependence on ventricular V1 receptors of the decreased luminal Cl − efflux when vasopressin was delivered via artificial CSF [45]. A transient increase in [Ca 2+ ] i in the choroid plexus epithelium was observed upon vasopressin administration [8], whereas vasopressin was without effect on choroid plexus cAMP [21]. This is in line with the presence of V1 rather than V2 receptors in the choroid plexus.…”

Section: Regulation Of Csf Productionmentioning

confidence: 81%

“…Interestingly, angiotensin II seems to act on CSF formation through the release of vasopressin from the choroid plexus to the ventricles [16]. This probably involved Ca 2+ signalling [8], as cAMP/ PKA induction by angiotensin II in choroid plexus was only reported for isoproterenol, prostaglandin, serotonin and histamine [21]. However, one preliminary report indicates that angiotensin II may also act on vasopressin release through cAMP/PKA [14].…”

Section: Regulation Of Csf Productionmentioning

confidence: 99%

“…Pflugers Arch -Eur J Physiol (2007) 454:[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18] …”

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Water and solute secretion by the choroid plexus

Prætorius

2006

Pflugers Arch - Eur J Physiol

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The cerebrospinal fluid (CSF) provides mechanical and chemical protection of the brain and spinal cord. This review focusses on the contribution of the choroid plexus epithelium to the water and salt homeostasis of the CSF, i.e. the secretory processes involved in CSF formation. The choroid plexus epithelium is situated in the ventricular system and is believed to be the major site of CSF production. Numerous studies have identified transport processes involved in this secretion, and recently, the underlying molecular background for some of the mechanisms have emerged. The nascent CSF consists mainly of NaCl and NaHCO(3), and the production rate is strictly coupled to the rate of Na(+) secretion. In contrast to other secreting epithelia, Na(+) is actively pumped across the luminal surface by the Na(+),K(+)-ATPase with possible contributions by other Na(+) transporters, e.g. the luminal Na(+),K(+),2Cl(-) cotransporter. The Cl(-) and HCO(3) (-) ions are likely transported by a luminal cAMP activated inward rectified anion conductance, although the responsible proteins have not been identified. Whereas Cl(-) most likely enters the cells through anion exchange, the functional as well as the molecular basis for the basolateral Na(+) entry are not yet well-defined. Water molecules follow across the epithelium mainly through the water channel, AQP1, driven by the created ionic gradient. In this article, the implications of the recent findings for the current model of CSF secretion are discussed. Finally, the clinical implications and the prospects of future advances in understanding CSF production are briefly outlined.

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Section: Regulation Of Csf Productionmentioning

confidence: 81%

Section: Regulation Of Csf Productionmentioning

confidence: 99%

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Water and solute secretion by the choroid plexus

Prætorius

2006

Pflugers Arch - Eur J Physiol

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“…CP cells were seeded at a density of 0.8 × 10 4 cells/cm 2 in a 24-well plate coated with type 1 collagen (Corning, Corning, NY, USA). Cells were cultured in DMEM/F-12 (Sigma-Aldrich, Saint Louis, MO, USA), 10% FBS (CCB, NICHIREI BIOSCIENCE, Tokyo, Japan), 10 mg/ml recombinant rat epidermal growth factor protein (R&D Systems), 1% Insulin/Transferrin/Selenium Solution (Thermo Fisher Scientific), and 1% penicillin streptomycin (PS) (Thermo Fisher Scientific) ( Battle et al., 2000 ). Cells were maintained in a 5% CO 2 incubator at 37 °C.…”

Section: Methodsmentioning

confidence: 99%

An enriched environment prevents cognitive impairment in an Alzheimer’s disease model by enhancing the secretion of exosomal microRNA-146a from the choroid plexus

Nakano

Kubota

Hashizume

et al. 2020

Brain, Behavior, & Immunity - Health

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Alzheimer’s disease (AD) is characterized by the extensive deposition of amyloid-β plaques and neurofibrillary tangles. We previously found that preserved function of astrocytes is associated with cognitively normal subjects with AD pathology. Here we show that an enriched environment (EE) can prevent cognitive impairment in AD model mice by ameliorating astrocytic inflammation and increasing synaptic density in the subiculum area of the hippocampus. In AD model mice treated with an EE, increased levels of microRNA (miR)-146a and down-regulation of NF-κB were observed in the hippocampus. In addition, increased levels of interferon (IFN)-γ were seen in serum from mice exposed to an EE. In vitro , enhanced miR-146a expression was observed in exosomes derived from the choroid plexus (CP) after IFN-γ treatment. In further in vitro experiments, we transfected miR-146a into Aβ/lipopolysaccharide-induced inflammatory astrocytes and showed that miR-146a ameliorated astrocytic inflammation by down-regulating tumor necrosis factor receptor-associated factor 6 and NF-κB. The present study indicates that following an EE, exosomal miR-146a derived from the CP cells is a key factor in ameliorating astrocytic inflammation, leading to synaptogenesis and correction of cognitive impairment.

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